Research has shown that decay accelerating factor (DAF) and other intrinsic complement regulatory proteins serve as shields to protect self cells from autologous complement-mediated injury. Additionally, research has shown that C5a and C3a receptors (i.e., C5aR and C3aR) play an important role in the attraction of phagocytic cells to immunologically engaged tumor beds and ingestion of complement opsonized tumor cells. Based on these findings, current approaches towards cancer therapy focus on blocking the activities of DAF and other intrinsic regulators so as to render tumors cells susceptible to killing, and on enhancing C5a-C5aR and C3a-C3aR interactions on phagocytic cells so as to increase their influx into tumor beds.